Lyall Laura M, Stolicyn Aleks, Lyall Donald M, Zhu Xingxing, Sangha Natasha, Ward Joey, Strawbridge Rona J, Cullen Breda, Smith Daniel J
School of Health and Wellbeing, University of Glasgow, Glasgow, UK; Division of Psychiatry, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
Division of Psychiatry, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
J Affect Disord. 2025 Apr 1;374:247-257. doi: 10.1016/j.jad.2024.12.069. Epub 2024 Dec 23.
Whether depression and poor sleep interact or have statistically independent associations with brain structure and its change over time is not known. Within a subset of UK Biobank participants with neuroimaging and subjective and/or objective sleep data (n = 28,351), we examined associations between lifetime depression and sleep disruption, and their interaction with structural neuroimaging measures, both cross-sectionally and longitudinally. Sleep variables were: self-reported insomnia and difficulty getting up; actigraphy-derived short sleep (<7 h); sustained inactivity bouts during daytime (SIBD); and sleep efficiency. Imaging measures were white matter microstructure, subcortical volumes, cortical thickness and surface area of 24 cortical regions of interest. Individuals with lifetime depression (self-reported, mental health questionnaire or health records) were contrasted with healthy controls. Interactions between depression and difficulty getting up for i) right nucleus accumbens volume and ii) mean diffusivity of forceps minor, reflected a larger negative association of poor sleep in the presence vs. absence of depression. Depression was associated with widespread reductions in white matter integrity. Depression, higher SIBD and difficulty getting up were individually associated with smaller cortical volumes and surface area, particularly in the frontal and parietal lobes. Many regions showed age-related decline, but this was not exacerbated by either depression or sleep disturbance. Overall, we identified widespread cross-sectional associations of both lifetime depression and sleep measures with brain structure. Findings were more consistent with additive rather than synergistic effects - although in some regions we observed greater magnitude of deleterious associations from poor sleep phenotypes in the presence of depression.
抑郁与睡眠不佳之间是否相互作用，或者它们与脑结构及其随时间的变化是否具有统计学上的独立关联尚不清楚。在英国生物银行中具有神经影像学以及主观和/或客观睡眠数据的一部分参与者（n = 28351）中，我们从横断面和纵向两个方面研究了终生抑郁与睡眠障碍之间的关联，以及它们与结构性神经影像学测量的相互作用。睡眠变量包括：自我报告的失眠和起床困难；通过活动记录仪得出的短睡眠（<7小时）；白天持续不活动发作（SIBD）；以及睡眠效率。影像学测量包括白质微观结构、皮质下体积、24个感兴趣皮质区域的皮质厚度和表面积。将有终生抑郁（自我报告、心理健康问卷或健康记录）的个体与健康对照进行对比。抑郁与起床困难之间的相互作用，对于i）右侧伏隔核体积和ii）小钳夹的平均扩散率而言，反映出在存在与不存在抑郁的情况下，睡眠不佳的负相关更大。抑郁与白质完整性的广泛降低有关。抑郁、较高的SIBD和起床困难分别与较小的皮质体积和表面积有关，尤其是在额叶和顶叶。许多区域显示出与年龄相关的下降，但抑郁或睡眠障碍并未使其加剧。总体而言，我们确定了终生抑郁和睡眠测量与脑结构之间广泛的横断面关联。研究结果更符合相加效应而非协同效应——尽管在某些区域，我们观察到在存在抑郁的情况下，睡眠不良表型的有害关联程度更大。
